Pacemaker rate control is conventionally derived from control signals obtained from a plurality of measuring elements such as cardiac catheters, special breathing sensors, body temperature sensors, etc. Functional parameters used for the control of the pacing rate are dependent upon both a patient's physical condition and dynamically changing parameters. It is desirable to have the pacing rate controlled by information derived from parameters truly representing the patient's physiological condition.
Some available publications describe pacing rate control of a pacemaker by measured signals based on the detection of one physiological functional parameter to provide pacing rate control dependent upon pulmonary activity. Thus, in U.S. Pat. No. 4,567,892, G. Plicchi, et al., Feb. 4, 1986, the respiratory rate is determined from an implanted secondary electrode by an impedance measurement. In U.S. Pat. No. 4,697,591, A. Lekholm, et al., Oct. 6, 1987, the respiratory rate is determined from impedance across the chest cavity by using the can and heart implant electrodes. In U.S. Pat. No. 4,596,251, G. Plicchi, et al., June 24, 1986, the respiratory minute volume is measured by impedance changes from an additional measuring electrode located in the chest cavity. Other related respiratory rate controls are effected in U.S. Pat. Nos. 3,593,718, J. L. Krasner et al., July 20, 1971; 4,721,110 M. S. Lampadius, Jan. 26, 1988 and 4,702,253, T. A. Nappholz et al., Oct. 27, 1987. In U.S. Pat. No. 4,576,183 G. Plicchi, et al., Mar. 18, 1986 subcutaneous electrodes in a patient's chest are used to measure impedance for control by a respiratory parameter.
Recently there have also been proposals to control the pacing rate of a cardiac pacemaker from two or more physiological functional parameters. In German Patent P 36 31 155 C2, published Mar. 24, 1988, pacing rate is controlled for stable long-term control from the temperature of the venous blood within the heart and from an activity sensor for short-term exercise related activity. The temperature signals can be modulated by the activity signals for an optimal adaptation of the pacing rate to the particular exercise of the patient. Different sensors may be used to check the two functional parameters. The pacemaker control is based on the finding that essentially only absolute values such as the blood temperature and activity should be used for determining a relationship between these parameters and the pacing rate, whereas other physiological functional parameters are merely relative parameters, which at least impede stable long-term control of the pacemaker. U.S. Pat. No. 4,722,342, D. Amundson, Feb. 2, 1988 provides a plurality of different body activity sensors to derive variable pacer controls for body activity.
Respiratory control of a pacemaker pulse rate with a respiratory signal derived from analyzing the stimulation pulse reaction on the already implanted pacemaker electrode is set forth in U.S. Pat. No. 4,694,830 issued to A. Lekholm Sept. 22, 1987.
U.S. Pat. No. 4,702,253, supra, discloses a metabolic-demand pacemaker in which the standby rate is a function of respiratory minute volume. This invention is based upon the finding that ventilation effects a change in the diameter of blood vessels in the immediate vicinity of the heart. The blood in the vessels comprises a volume conductor, and its impedance is measured by establishing a known current field and measuring the voltage which develops in the field. Preferably, the voltage is measured between the high right atrium or the superior vena cava and the pacemaker case, whereby the superior vena cava is assumed to be the ideal vessel for use. The modulation in the impedance measurement is assumed to be a direct measure of minute volume. A linear relation of the degree of impedance changes in the superior vena cava to minute volume is assumed to be present. By summing the values of the degree of impedance changes, a direct measure of minute volume is assumed to be obtainable to serve for control of the pacemaker rate. It is shown hereinafter that corrections must be made for non-linearities in order to properly control the pacemaker rate.
According to the prior art, the change in thoracic impedance was determined between an implanted pulse generator can in the chest and the tip of a secondary electrode in the heart. The basis for these measurements is the empirical fact that breathing causes a change in impedance as the sum of a plurality of cumulative resistances. Each individual tissue and its corresponding share of resistance has a corresponding influence on a total impedance. Various body tissues with their individual impedances have a corresponding share of the total measured value. The greatest influence is exerted by blood, lung, fatty tissue, connective tissue and myocardium, including the transition impedances between two adjacent tissues. Both the transition impedances and the impedance of the fatty and connective tissue are largely independent of respiratory and cardiac activity. Thus, they influence the absolute value of total impedance but do not make any essential contribution to its fluctuations due to breathing and heartbeat activity. Regarding the variation of intrathoracic impedance alone, blood and lung are decisive as the main influencing variables. In accordance with the predominance of lung tissue, impedance fluctuations occur when impedance changes are determined between a pacemaker can and the tip of a secondary electrode implanted above the right hemithorax. These fluctuations are mainly due to a change in the distance between the two measuring points and to a decrease or increase of lung structure due to respiratory activity.
Comparing the various individual impedances of the human body with varying electrical conductivity, impedance resistance Z measured between two points is determined by the particular share of resistance tissue with the specific resistance R, length L and the particular cross-sectional area A. Thus Z=RA/L. Regarding the thorax as a volume body, Z=RL.sup.2 /V.
These theoretical considerations make it clear that measurements between the pacemaker can and the tip of a routinely used stimulation electrode show impedance changes due to breathing which are determined by the events of the heartbeat, blood circulation and by respiratory activity. The relatively low specific resistance of blood is the major influencing factor in impedance measurements, since it has a specific resistance of approximately 100 ohms times cm at a hematocrit of 45%, compared to the lung with approximately 1000 ohms times cm. It is clear that the total impedance only changes slightly due to breathing in spite of the predominant volume of the lung in measurements in the area between the pacemaker can and the tip of the stimulation electrode. Also, the cardiac and circulatory fluctuations behave contrary to the pulmonary impedance fluctuations and thus virtually compensate for pulmonary fluctuations. This is due to the increase of lung impedance due to inhalation, on the one hand, and to the drop of intracardiac, intravascular and hilar (vessels of the root of the lung) impedance due to inhalation within the measured path between the tip of the stimulation electrode and the pacemaker can, on the other hand.
These theoretical considerations have been proven and supported in numerous experiments. It was additionally shown that the change in volume of the superior vena cava, which clearly responds in particular to the patient's change of position, is an important determinant value for impedance. It was also shown that in measurements in which the superior vena cava is located in the measured path to the pacemaker can, the changes in volume and diameter of the superior vena cava due to speaking, and thus the changes in the resistance value of the low-impedance blood column of the superior vena cava are even predominant compared to the changes in the lung due to breathing. The concept aimed at by other investigators of determining respiratory activity by determining the thransthoracic changes of impedance between the cardiac apex and the pacemaker can, is therefore, according to our tests, very susceptible to disturbance compared to non-ventilation influences such as pressing, coughing, speaking, laughing and sudden changes of position. Furthermore, the relation is unfavorable between the information signal--breathing--and the interference signal--the above mentioned influences not due to breathing.
Previous tests for determining the transthoracic impedance fluctuations due to breathing assumed that an increase of thoracic impedance must be expected inspiratorily due to increased inspiratory lung tissue of high impedance. Our investigations showed that determination of the lung impedance changes due to breathing often leads to incidental and unstable results due to changes resulting from blood volume. Furthermore, we found that the simultaneously determined cardiac and circulatory changes of impedance in transthoracic measurement do not have any directional and reproducible valence, i.e., they are of only limited value for an implantable pacemaker system. This especially holds true if the amplitude of the ventilation of the patient is to be detected from the amplitude of those impedance measurements.
Accordingly, problems not solved by this typical prior art, must be considered and overcome, such as the detection of low level signals that may be masked in the presence of stimulation pulses, as in Lekholm, supra. Further, the presence of multiple electrodes provide probable interference and error depending upon positioning and are generally not feasible when implantation is required. For example, when considering pulmonary activity, critical to dynamic changes of a patient's physiological parameters necessary for pacing rate control, measurements in the chest will introduce significant errors in the presence of motion, coughing, sneezing, laughter, etc. which make pacing rate control from such signals responsive to undesired sensed conditions not a function of continued exercise or exertion, which are otherwised detectable from pulmonary activity. Other sensing systems, such as with body temperature, introduce time delays so that a very accurate dynamic real time control is not feasible.
Therefore, it is an object of this invention to provide more reliable determination of a patient's minute ventilation.
A further object of this invention is to provide control of pacing rates tailored to respond to individual exercise and respiratory characteristics of a patient, rather than to rely solely upon instantaneously sensed parameters.